The following results have been obtained in the last year: (1) The resorcinol bronchodilators, terbutaline (TERB), alupent (ALU) and fenoterol (FEN), do not interact at the same site(s) that the catecholamine and catecholamine-like drugs interact, norepinephrine (NE), epinephrine (EPI), isoproterenol (ISO) and salbutamol (SAL). (2) Since SAL is considered a Beta 2-agonist and NE a Beta 1-agonist, and the dissociation constants (KB) for the propranolol-Beta-receptor complex were calculated to be identical using these agonists, the terminology of Beta 1 and Beta 2 receptors do not sufficiently differentiate these sites in the rat trachea. (3) The resorcinol drugs apparently do not interact at either a Beta 1 or Beta 2 receptor in the rat trachea, even though by definition, these drugs seem to primarily affect organ systems defined as Beta 2-mediated systems. And (4) There is an important interaction between these sites, since TERB will cross-densensitize the catecholamine receptors and vice versa. Studies done with the new "irreversible" Beta-receptor antagonist drug N-(2-hydroxy-3-(1-naphthyloxy)-propyl)-N'-bromoacetyl-ethylenediamine (NHNP-NBE) strongly suggest the presence of a very large "spare"-Beta-receptor population in rat tracheal smooth muscle. Using the guinea-pig trachea, we have found that the steroid methylprednisolone potentiates the bronchodilator effects of catecholamines but does not do so by increasing receptor affinity. Studies in the third year will include an attempt to isolate and culture rat and/or human tracheal (bronchial) smooth muscle cells. This will be attempted in order to measure receptor binding characteristics in a purified cell preparation thus minimizing non-specific binding.